Change in the microviscosity of cell membranes were shown to modulate the functionality of their receptors, presumably by altering their ability to reorient into more or less active positions. 1) The abnormal accumulation of saturated long chain fatty acids in the inherited disease of adrenoleukodystrophy also result in stiff membranes for when human adrenocortical cells are cultured in their presence, 15 times more ACTH is needed to achieve level of cortisol synthesis. This probably explains the mechanism by which adrenal insufficiency occurs in this disease. 2) Gossypol is a dietary phenolic that has caused outbreaks of infertility in several provinces in china. This compound causes an increase in granulosa cell membrane microviscosity and thereby decreases their estrogen response to FSH. Altered functionality of gonadotropin receptors on target tissues is a likely mechanism by which this phenomenon of infertility occurs. 3) We have shown that the unique 19OH prostaglandins in human semen suppress lymphocytes' response to mitogens 30 times more than PGE2. Preliminary studies demonstrated that they reduce the microviscosity of human lymphocyte membranes, a phenomenon that may be extremely important in explaining the increased susceptability of homosexuals to various infective agents. Other preliminary studies have shown that these same prostaglandins cause a marked decrease in the microviscosity of human membranes, an observation that may be relevant to their role in male reproductive physiology. A direct link between the immune surviellance system and the adrenal gland was established when human monocytes were shown to elaborate a soluble factor that stimulates human adrenocortical cells to synthesize cortisol in vitro. Preliminary studies have indicated that the monocytes and granulocytes of diabetic patients metabolize arachidonic acid in an abnormal fashion. The identity of these metabolites is being established and the possible role in the microvascular disease of diabetes is being studied.